Abstract
In 1978, Krauthammer and Klerman [1] elucidated the concept of secondary mania. This refers to the occurrence of symptoms which meet the diagnostic criteria for mania produced by neurological, metabolic or toxic disorder. Since then, several authors have discussed the implication of mania arising for the first time in late life [2–4]. Late-onset mania is rare and most authors acknowledge comorbid neurological disorder and low rates of familial affective disorder in this group.
Post-stroke depression is a common condition and has been the focus of considerable research [5]. In contrast, mania after stroke has rarely been noted [6]. Dunne et al. [7] identified only three cases of post-stroke mania among 661 stroke patients, and similarly Starkstein et al. [8] identified three cases in their series of 700 consecutive stroke patients. Most of the reported cases had lesions in the non-dominant hemisphere. Up until late 1996, there have been only five case reports in the literature of post-stroke mania or bipolar disorder arising from left hemisphere lesions [9].
We report a sixth case of secondary mania late in life following a stroke involving the left hemisphere.
Case history
Three weeks prior to hospitalisation RS, a 78-year-old, right-handed man was over-active, erratic and disorganised. He embarked simultaneously on a number of household maintenance tasks. During the same period his capacity for self-care deteriorated dramatically. He was not eating regularly and his house was in a mess. An ongoing argument developed with his neighbour with whom he was on excellent terms previously.
RS locked himself out of the house the day prior to hospital admission. His daughter was concerned and took him to the local hospital. RS was initially admitted to a medical ward. Following investigations, as RS insisted on going home he was admitted to the adult psychiatric unit as an involuntary patient with a diagnosis of hypomania. On the psychiatric ward, RS remained over-active, irritable and unable to sleep. Haloperidol (1.5 mg b.d.) and sodium valproate (200 mg b.d.) were commenced and after 36 h, RS was transferred to the psychogeriatric unit.
RS had no past psychiatric history but was being treated for hypertension by his general practitioner for 10 years. There was no family history of psychiatric disorder.
On admission to the psychogeriatric unit, RS had an irritable and elevated affect. He stated feeling ‘great’. There was mild pressure of speech and he expressed himself volubly. The rate and volume of speech were increased. Thought was circumstantial and disorganised with intermittent flight of ideas. RS was alert and there was no clouding or fluctuation of his consciousness. He was correctly orientated in place and person but disorientated for the day and date. Attention and concentration were significantly impaired. Short-term memory was impaired. Long-term memory for personal and non-personal events was accurate. Comprehension and expressive command of language was intact. Simple arithmetic tasks were easily completed. Tests of visuospatial function revealed moderate deficits. Abstract reasoning was intact. Executive planning was impaired and he had dressing dyspraxia.
RS walked with a limp favouring his right leg. System examination was normal. His pupils were equal and reactive to light. Visual fields were normal. Examination of the fundi showed silver wiring of the major retinal arteries. There were no retinal infarcts or haemorrhages observed. There was no diplopia or nystagmus to lateral gaze. Examination of the remaining cranial nerves was normal. An examination of the upper limbs revealed normal tone, power, reflexes, coordination and sensation. In comparison with the left leg, there was weakness of the right hip flexion, graded as 4/5. Tone in both lower limbs was normal. The reflexes of both limbs were brisk, but symmetrical. The plantar reflexes were normal. There was mild hyperaesthesia over the proximal, lateral aspect of the right thigh. Coordination of the right leg was impaired, and this was felt to be attributable to the weakness of hip flexion.
Full blood count, urea, creatinine, electrolytes, liver function test, random glucose, thyroid function tests, B12 and folate levels, syphilis serology and urinalysis were all within the normal range. An electrocardiogram revealed sinus rhythm with right bundle branch block but was otherwise normal. Chest X-ray was unremarkable. Computed tomography (CT) head scan without contrast revealed ‘mild cortical atrophy with focal atrophy in the left parietal cortex’; CT head scan with contrast revealed ‘low density infarcted areas involving the left subinsular cortex, the left external capsule and the left frontal and high left parietal cortical areas’; and CT head scan repeated 4 weeks later without contrast revealed ‘small focal areas of infarction within the left basal ganglia and a recent area of infarction in the left insular region’. A single photon emission computed tomography (SPECT) scan would have given more information but unfortunately SPECT scans are not done routinely on our patients and we did not consider this at that time.
The report from the neuropsychologist assessment 3 weeks after admission was summarised as follows: ‘mild to moderate impairment of recent memory and new learning, visuospatial function, planning and insight, against a background of otherwise well preserved neuropsychological function. Such a picture of patchy cognitive deficits with an apparently sudden onset is most consistent with a vascular aetiology. Emotional lability and disorganized behaviour may also result from this, particularly when left frontal regions are involved’.
RS experienced severe insomnia along with grossly disorganised behaviour on the Psychogeriatric Unit (PGU). Two days prior to his admission to the PGU, he was started on haloperidol (1.5 mg b.d.) and sodium valproate (200 mg b.d.) on the adult psychiatric unit. Shortly after admission, RS developed an erythematous, maculopapular rash over his arms, trunk and lower limbs. Sodium valproate was ceased and the skin rash resolved. RS also began to hyper-salivate and the haloperidol was tapered off. To help with his insomnia and grossly disorganised and intrusive behaviour, lorazepam (0.5 mg b.d.) and thiori-dazine (20 mg nocte) were started.
Over a 2-month period, his elevated mood settled to an euthymic level. The disorganisation gradually improved. Following occupational therapy assessment, RS was discharged to supported accommodation. His improvement continued and after 2 months, following further occupational therapy assessment, it was felt that RS was capable of independent living. A repeat neuropsychological assessment confirmed considerable improvement in all areas of cognitive function. All areas of performance fell within the normal range or above and no residual impairment in cognitive function was identified.
Discussion
RS presented with a mania after stroke of the left insular cortex and left basal ganglia.
His mania arose suddenly without pre-warning and concurrently with a sudden onset of weakness and paraesthetic sensation in his right leg. There was clear radiological evidence of left-sided cerebral cortical and subcortical infarction noted to be of recent onset and consistent with the right-sided weakness. There is a temporal relationship between cerebral infarction, physical paresis and the mania. The evidence of a physiological relationship between RS's stroke and mania is strengthened by the atypical features of his mood disorder, absence of a family history and absence of a past history of mood disorder [2].
Robinson's group in Baltimore has published extensively describing an association between major depression and strokes located in the left frontal areas and left basal ganglia. Starkstein and Robinson have extended this work ascribing lesion locations to the full range of post-stroke neuropsychiatric syndromes [10]. More recently, they have sought to elaborate the mechanisms behind these syndromes relating lesion locations to postulated neuroanatomical function and disruption of neural networks [11],[12]. Starkstein et al. [8] found in their study that brain lesions in patients who later developed secondary mania were mainly located in limbic or limbic-related areas that have strong connections with the frontal lobe. They also suggested a strong association between secondary mania and lesion to the right hemisphere [8],[12]. But other authors are less convinced by the argument for non-dominant cerebral laterality in the genesis of manic disorder, in particular, or mood more generally. Liu et al. [9] conclude in their discussion that it is presumptive to consider mania a syndrome of the right or non-dominant hemisphere alone.
Evans et al. [13] note the difficulty of treating late-onset mania with traditional antimanic medication, particularly lithium. They suggest this problem arises first from the general sensitivity aged patients exhibit to psychotropic drugs. The presence of neurological disease further impairs drug tolerability and reduces psychotropic efficacy. RS tolerated poorly low doses of haloperidol, thioridazine and sodium valproate. It is doubtful whether the eventual resolution of symptoms was attributable to pharmacological intervention to any great extent.
Footnotes
Acknowledgements
We would like to thank RS, who consented to this case history being written, and acknowledge the staff of the Psychogeriatric Unit, North-west Hospital. We also thank Associate Professor David Ames for his helpful comments and Ms Janet Tully for help with the word processing.